Lets look at the above medications. Tell me what you know about them.
What are the pharmacological properties of each of these?
How do they interact with one another?
Why are they given to patients with diabetes?
Why are patients with diabetes prone to CVD?
Do any of these exert any oral effects? If so, how does an OHT manage these?
Lets get some serious discussion happening around these key questions.
Subscribe to:
Post Comments (Atom)
Metformin: antidiabetic. decreased blood glucose by decreasing hepatic glucose production. also decreases intestinal absorption of glucose and icnreased response to insulin. Used as an adjunct to lifestyle changes in type II diabetes pt.
ReplyDeleteNorvasac: Ca channel blocker. Reduces cardiac output thus reducing bp. Side effects include gingval hyperplasia (rare), dry mouth. Be aware of postural hypotension.
Crestor: antihyperlipademic. Used to tx pt with atherosclerosis and high BP. Stops synthesis of cholesterol with proteins to form transporable lipoproteins.
I dont think they interact with each other, but I have been wrong plenty of times before!
Pt wtih diabetes (particularly typeII) are prone to CVD as they share many common risk factors as they have links to lifestyle factors. For example pt with diet high in LDL is susceptible to atheroscleroris.
To mange the effects of these meds, encourage increased consumption of water, and also provide OHI to show how to adequately clean and manage gingiva to ensure no inflammation
Looking good Tom. Ok now lets look at what happens on a histological level in diabetes and why this predisposes them to CVD. I agree with lifestyle factors as you have pointed out but lets list how diabetes affects the CV system hence the need for BP meds.
ReplyDeleteGood stuff Tom! Sorry for any spelling mistakes gang, i've blown our Internet quota through the roof this month and now have to use my iPhone to type answers!!
ReplyDeleteJust adding onto Tom's answer, the aspect of pts with diabetes being more prone to CVD is also associated with the involvement of the illusive AGE macromacromacro molecule! Remember that in PTs with DM, hyperglycaemic conditions pertain to glucose molecules attaching to surrounding tissues and cells and proteins forming 'irreversibly glycated' (sticky) compounds called 'advanced glycation end products' (AGE). AGE is a menace to both the endothelium and the periodontium!
In a nutshell, excess AGE binds to collagen, thereby encouraging increased collagen crosslinking to form macromolecules that are resistant to both breakdown by proteolytic enzymes and movement throughout the blood vessels. As a result, these macromolecules accumulate in the blood vessels, increasing the thickness of the BV wall, increasing the total peripheral resistance (blood pressure), and attracting high levels of LDLs (low density lipoproteins) which can put a patient at risk of atherosclerosis!
As a side note particularly relevant for perio patients, this AGE also binds toendothelial cells, thus increasing the thickness of the basement membrane (that lies over the VASCULAR Cx tissue) thereby altering/preventing nutrient transport across the membrane to encourage wound healing!!
That's great guys, a huge help, sounds spot on...
ReplyDeleteJust a couple of things to add regarding the medications and interactions.
As HanB said with the risk of increase in TPR and artherosclerosis, this would explain the prescription of Norvasc to decrease BP and Crestor in lowering LDL levels.
Norvasc is a calcium channel blocker decreasing the force of contraction by blocking calcium channels during plataeu of action potential -> increases vasodilation -> decreases TPR -> decreases BP.
Crestor inhibits the enzyme (HMG-CoA reductase) responsible for producing cholestrol. Increasing liver cholestrol uptake from blood -> decrease LDL, increasing LDL.
One potential side effect of Crestor is an increase in BGL which could potentially contribute to hyperglycaemic conditions therefore stabilising BGL is crucial.